You say chee•lay•shun, I say kee•lay•shun. For whatever reason, that first pronunciation makes me think of Chia Pets and that catchy song “Ch-ch-ch-chia” (you can thank me later for sticking that in your head for the day). But the second, and correct, pronunciation makes me think of a “key” to detoxification and to your overall health. Now that sounds like something worth talking about.
What is chelation?
Chelation is a therapy for removing heavy metals such as lead, arsenic, aluminum, mercury, and cadmium from the body by attaching them to a chelator. A chelator has a unique structure within which there is a baseball mitt-like pocket with a magnetic charge that attracts and binds these toxic metals. In our clinic we use both natural and pharmaceutical chelators and they can be administered in many forms, but for the purpose of this article we will only be discussing IV chelation with EDTA.
EDTA is a pharmaceutical chelator and is essentially a synthetic amino acid. You may not have heard about the drug EDTA, but you have most definitely swallowed it as it is used in our food because it also acts as an anti-oxidant and keeps food (even fresh broccoli) from losing it color to oxidation. There are two forms of EDTA: Disodium EDTA (NaEDTA) and Calcium EDTA (CaEDTA). NaEDTA has FDA approval for treating hypercalcemia, while CaEDTA has FDA approval for treating lead poisoning.
Who can benefit from chelation?
Well, if you go strictly by these FDA approved uses, I have probably had only two patients that would have qualified in the last five years. However, I recommend chelation a couple times a week due to the vast number of conditions that I, and many other chelating doctors, have seen improve with this therapy. In our clinic, if I suspect that heavy metal burden is contributing to your health issue, I will recommend we do a test to get a picture of what your metal burden is and based on the results and your clinical history/risk factors, we will decide if your health problems are likely to be improved in a major or minor way by removing them. IV Chelation is the fastest, and often the best, method available.
Will It help your heart?
Besides its established use for removing metals, IV chelation with EDTA is frequently used by chelating doctors for heart disease and circulatory problems. It is thought to be especially helpful if the patient is diabetic or a smoker. However, these claims of improving cardiovascular disease are by far the biggest controversary surrounding chelation as an alternative therapy. Let’s look specifically into this controversial topic, starting with a little historical background…
How It All Began
(This is the “Dr Wellsian highly-condensed, hit-the-highlights and throw your own 2 cents in at the end” version. For a much more thorough timeline, please follow this link.)
EDTA was first created to fill a need in the textile industry to remove calcium as part of textile processing. A patent for this was filed in Germany in 1935. In the 1940’s Martin Rubin PhD, a professor at Georgetown University, discovered its use as an anticoagulant, for which it is still used today in laboratory tubes (in the form of potassium EDTA). He continued to collect literature of its uses and was instrumental in getting it approved by the FDA for lead poisoning (CaEDTA) and hypercalcemia (NaEDTA) in the 1940’s. In the 1950’s, doctors who were using EDTA for the FDA-approved purposes documented and published articles noting improvements in these same patients’ heart disease. In the 1960’s, investigation picked up, but due to a series of unfortunate events, further investigation became discouraged. When the pharmaceutical company’s patent ran out in 1969 there was little financial motivation to further promote EDTA as a treatment for heart disease. In 1973, the American College for the Advancement of Medicine (ACAM) was formed to teach and promote chelation therapy, and it still exists today as the premiere promoting and training institution, but despite continuous efforts over the next four decades, and many published papers showing positive results, chelation continued to be largely ignored and discounted.
Personally, I believe the major blow was brought on in the late 70’s by the new theory on the block…cholesterol causes heart disease.
In 1977 our government announced their recommendation for all Americans to eat less fat. This ideology was completely solidified by the early 1980s. 1987 brought the first FDA- approved statin medication and cardiology hasn’t looked back since! But it may be forced to soon…
Jumping forward to 2013, we now have the TACT: Trial to Assess Chelation Therapy. Thanks to the unrelenting effort by ACAM and the plethora of papers brought as evidence of the effectiveness of chelation for cardiovascular disease, the NIH finally conceded that a large-scale random controlled clinical trial would be funded.
What is the TACT?
The trial consisted of 1708 patients aged 50 years and older who had a prior heart attack. Half of the patients were given 40 IV chelations with EDTA while the other half were given saltwater placebos over the course of about 1 year. Outcomes were followed for 5 years after onset of treatment. The study, including follow-ups, lasted nearly a decade and involved 134 medical offices for a total of 55,222 IV infusions! Fought all the way through by it’s dissenters as a waste of 30 million dollars, and conducted by several investigators that openly admitted that they had hoped it would disprove chelation as a therapy once and for all, the TACT results were published in 2013 for the world to see.
What were the TACT outcomes?
According to the principle investigator Gervasio Lamas MD, a leading cardiologist at Mount Sinai Medial Center and a former dissenter himself, the results showed:
- Overall, there was an 18% reduction in heart events (death, another heart attack, bypass/stenting, stroke, or even hospitalization for chest pain) in the EDTA group as compared to placebo.
- When the group that did the IV EDTA and oral vitamins was compared to placebo the reduction in these events went to 26%.
- Most impressive was the effect in diabetic patients in whom there was a 41% reduction in all events, including 43% reduction in death, specifically!
Consider that these results were for a 5-year period and the IVs were completed in just over a year, so the effect was lasting. There is no intervention close to comparable to these results in all of conventional diabetic therapies! In other words, EDTA would be a blockbuster drug if there was still a patent.
So, how does it work?
The short answer is that we are still trying to figure this out, but there have been two major theories proposed. The original theory was simply that since we know that EDTA was created to remove calcium from textiles, that it could be removing calcium from the atherosclerotic plaques on the walls of the arteries causing them to be less thickened/stiff (i.e. more pliable means better blood pressure and blood flow). It was also thought that removing this calcium “infrastructure” allowed the body to dissolve and reduce the plaque burden on the walls. Most of the clinical improvement seen was related to better perfusion of areas previously ischemic and better blood pressure which fit this model. 90% of EDTA is excreted in the urine with whatever it is bound to, so a study was conducted that measured the difference between normal daily urine calcium losses and post chelation levels. The difference was astoundingly low and could not be enough to explain the results they were getting. So then they theorized that perhaps the shift in blood levels of even that small amount of calcium over such a short period was enough to trigger the release of parathyroid hormone (PTH), which regulates blood calcium levels and calcium moving from blood to bone and vice versa. If changes in this hormone induced even greater amounts of calcium to be moved to normal storage places like bone rather than just excreted, this could be enough to explain the changes expected in the calcium deposit theory of chelation.
The newer theory that is more favored by most chelation doctors is the idea that EDTA’s original medical use, the removal of heavy metals, is the cause for the improved cardiovascular effects. Though studies looking at the effects of metals on the human body have mostly focused on the neurological effects (not cardiovascular) and short-term high-dose exposures (toxicity or poisoning), we do know that mercury and lead poisoning cause hypertension and we know that the two basic ways that metals cause damage in the body are by inducing free radical production (oxidative damage) and by attaching to enzymes (jamming up their functionality). And so compelled by this newer theory and a growing concern over the toxicity of our environment – contaminating us with metals and other chemicals – scientists asking new questions and revealing some profound findings…
In a review article done Brazilian scientists entitled “Toxic effects of mercury, lead, and gadolinium on vascular reactivity”, the authors summarize the emerging body of evidence showing the effects of chronic low-doses of these metals on the cells of our arterial walls, called the endothelium. First, they state that “Vascular endothelium is highly sensitive to oxidative stress and this is the cause of endothelial dysfunction observed in cardiovascular diseases such as hypertension and atherosclerosis.” In fact, recent studies show that increased arterial pressure has been reported in individuals with as little as 31.4 ug/dL of lead in their blood. This falls well below the acceptable range of 40 – 60 ug/dL for non-occupationally exposed people in Brail, leading the authors to argue for a re-evaluation of current standards for acceptable blood levels. Importantly, though both high levels and low levels of metals can affect the cardiovascular system, the mechanisms may be quite different. For example, in acute mercury exposure, heart muscle contraction is reduced by the blocking of an enzyme called myosin ATPase (i.e. in acute poisoning your heart just stops pumping), whereas in chronic exposure to lower levels of mercury, vascular resistance increases. Mercury does this by increasing local vasoconstriction and decreasing nitric oxide - our natural vasodilator released by the endothelium (i.e. it causes vessels to clamp down and blocks the un-clamp signals!) It also depletes glutathione (our major anti-oxidant) allowing oxidative damage to blood vessel walls. This damage must be smoothed over quickly to maintain good flow of red blood cells so our body lays down plaque over the damaged areas to patch up the “hole”. Thus it is likely inflammatory (oxidative) damage that is the true cause of atherosclerotic plaque formation, and NOT the amount of cholesterol you have in your blood!
The mechanisms for lead are similar to mercury (leading to endothelial-induced vascular resistance), but also include affecting the autonomic nervous system (increasing sympathetic activity and reducing parasympathetic) thus causing the nerves that control vascular resistance to induce hypertension. Gadolinium (a metal used medically in recent years in contrast dyes for MRIs and CT scans) is known to cause nephrotoxicity (kidney damage) at high levels , but at low levels (i.e. what is left inside of you for years following such a study) it causes disruptions in ATP signaling both inside and outside of cells. ATP controls endothelial cell growth (think repair) and vascular smooth muscle growth and vasodilation.
Gadolinium also affects ACE enzyme activity which is a major player in how your kidneys work to regulate blood pressure (increasing it at low levels). Through its amplifying effects on ACE, it also can cause thrombosis, inflammation and vascular and heart thickening. (Note that high gadolinium levels block ACE activity, thus kidney damage occurs instead!) And when ACE inhibitors like Lisinopril (a blood pressure medicine) were used, these detrimental effects of the metals were blocked. So, is your cardiologist treating you for high blood pressure or is he/she unwittingly giving you blood pressure meds to treat your heavy metal burden?! Something worth thinking about…
The authors also point out that, though these adverse effects of gadolinium are now known, gadolinium has yet to be officially defined as a toxic agent and currently no recommended exposure limits have been defined.
One last nugget I’d like to share from this fascinating article is that when phenylephrine (e.g. the medicine Sudaphed®, which acts like the sympathetic system to increase stress response) was added to the metals the vasoconstriction response was increased. In other words, stress compounds the effects of toxic metal burden! And when the researchers removed the endothelial lining from the blood vessels in these laboratory studies, the effects of both the metals and the phenylephrine were abolished. The authors emphasize that this proves the endothelium, along with the signals it is releasing, are directly responsible for all of the cardiovascular effects of the metals. Therefore, if chelation brings cardiovascular improvements, it is almost certainly done by removing the metals directly from the endothelium (thus abolishing the effect of those removed metals), and if metals can be removed faster than they are accumulated (e.g. with chelation) one would expect to find a lasting effect such as was found in the TACT! Of final note, besides metals, the other huge cause of oxidative stress on blood vessels is elevated blood sugars (diabetes) so a greater improvement would be expected in this already higher risk population, as was the case in the TACT!
Impact and limitations of the TACT
Despite all of this compelling data, all we have to show for it is a change in the current guidelines for stable ischemic heart disease from a Class III recommendation (never do) to Class IIb (probably not effective). The study did fail to enroll the numbers that it had originally sought, so statistical significance for non-diabetics was not quite reached. Also, the study did not include patients with milder statuses of CVD to determine if the effects would be greater if started earlier in disease process, or less dramatic. It’s also important to note that all were given statins and none were advised in dietary changes other than standard heart health wisdom. Importantly, none of their hormones, or sleep, or other important factors were addressed like we do here at WHCH. I believe that chelation, along with the entirety of your health improved, will lead to much higher reductions in cardiovascular events. Thankfully, TACT #2 has been funded and is currently underway!
I really feel that the research is not long in bringing more clarity to this controversy and I hope you see why I believe that one day the notion of needing regular chelation treatments will be accepted in a similar fashion to needing regular dental hygiene visits. And I am so grateful to know that even as we work to reduce our environmental toxic exposures, we have chelation as an option to combat that which we cannot avoid!
From my heart to yours,
- Escolar E, Lamas GA, Mark DB, et al. The Effect of an EDTA-based Chelation Regimen on Patients with Diabetes Mellitus and Prior Myocardial Infarction in the Trial to Assess Chelation Therapy (TACT). Circ Cardiovasc Qual Outcomes. 2014; 7(1):15-24.
- Vassallo DV, Simoes MR, Furieri LB, et al. Toxic effects of mercury, lead, and gadolinium on vascular reactivity. Barz J Med Biol Res. 2011; 44(9):939-946.
- Lamas GA. Chelation Therapy: A new look at an old treatment for heart disease, particularly in diabetics. Circulation. 2015; 131:e505-e506
- Chappell T, Trowbridge J, Schachter M. A Timeline for Intravenous Disodium Edetate (chelation) as a Treatment for Vascular Disease. chelation.me
- Lanza GA, Crea F. Stable ischemic heart disease: The update to the 2012 guldeline. 2015; acc.org.